Much of the public’s attention regarding the rising incidence of obesity and issues related to weight control in general has been focused on good foods vs bad foods. Most popular diets are based upon the premise that the kinds of foods one eats is a dominant factor in determining weight – low carb vs low fat, for example.

Meanwhile, there is a growing body of scientific evidence, approaching consensus, that by far the dominant factor in weight control is the amount of calories one consumes, not the form in which those calories come. The best science-based nutritional advice for weight control seems to be – exercise regularly and practice portion control. For other health concerns, like heart health and avoiding diabetes – eat a well-balanced diet and get more of your calories from plants than animals.

That’s it in a nutshell, but it is hard to sustain a multi-billion dollar weight loss and self-help industry with such simple advice.

Further, it is human nature to prefer quick fixes and easy answers to tough love. Weight control is not complex, but it turns out to be very difficult for most people. Will power is not enough for 95% of the population. We can hardly blame people for what appears to be almost universal human traits. As a public health issue, approaches to obesity are not going to be found in scare tactics and weight loss schemes. The culture needs to change.

Part of that cultural change, in my opinion, is getting away from the very notion that the problem is caused by “bad foods”. The latest target of this approach is high fructose corn syrup (HFCS). As reported by Consumer Reports:

In 2004, researchers from the Louisiana State University and University of North Carolina published a paper that theorized that high-fructose corn syrup in beverages could play a role in the obesity epidemic. They looked at the correlation between the 1,000 percent increase in high-fructose corn syrup consumption between 1970 and 1990, and a correlating rise in obesity rates. Because of the way the body metabolizes fructose from beverages, the researchers argued, it may play a role in the obesity epidemic.

Of course, this was a classic example of confusing correlation with causation. The rising rate of obesity correlates with an overall increase in calories, and there is no evidence to implicate any particular source of calories as being the culprit.

Simple chemistry helps put HFCS into some perspective. Table sugar is sucrose, which is a combination of fructose and glucose – two common simple sugars. Corn syrup is mainly glucose, but HFCS is manufactured to have about 50% fructose and 50% glucose – the same ratio as sucrose or table sugar.

There are metabolic differences between fructose and glucose. Often studies showing that pure fructose can alter sugar and fat metabolism are presented as evidence against HFCS, missing the point that the ratio of fructose to glucose in the American diet has not changed with the introduction of HFCS.

A recent review of the literature published in the Journal of Nutrition, regarding the association of HFCS and obesity, concluded:

The panel concluded that evidence from ecological studies linking HFCS consumption with rising BMI rates is unreliable. Unlike some prominent epidemiologists, the expert panel concluded that the evidence from epidemiologic studies and randomized controlled trials is inconclusive. They also noted that there were inadequate data available that distinguish between HFCS consumption and sucrose consumption with respect to weight gain. Further, they acknowledged that while the sweetener level and type have changed over time, the fructose:glucose ratio in the U.S. food supply has remained the same for 50 y. Finally, the panel concluded that HCFS did not contribute to weight gain any differently than other energy sources.

In other words – HCFS is not the boogeyman. It is a distraction from the real issue – an increase in overall caloric intake. There may also have been a rise in total sugar intake, but the types of sugars have not changed. A diet with a large proportion of simple sugars is not a good idea because such a diet is also likely to contain too many calories, and high sugar intake increases the risk of diabetes.

Now, of course, the corn lobby is hard at work promoting this information – that HFCS is not the bad guy. But don’t make the mistake of assuming that because some information is in line with the interests of a specific corporation or industry that means the information is false. Any such information is likely to have winners and losers, that doesn’t mean it’s a conspiracy of the winners. We could just as likely conclude that negative information about HFCS is a conspiracy of the sugar cane lobby.

This does mean that we have to look for corporate interests in the published scientific data, and demand full disclosure of any potential conflicts of interest. There doesn’t appear to be any in the literature I reviewed – it seems there is a broad based consensus, not just corporate shills. I’m sure this won’t stop some from accusing me of being part of the corn lobby.

The bottom line is that HFCS is sugar. It is high calorie and has no other nutritional value other than as fuel. It should be consumed, like all sugars, in moderation. People should be aware that HFCS = sugar, and not be confused by this on food labeling.

But we will not impact the rise in obesity by treating HFCS as the culprit, or by replacing it with other sugar-based sweeteners. We need more evidence-based public health measures to fight obesity – making healthy choices easier, making portion control easier, and disclosing calories on menus so that people know how many calories they are consuming. We don’t need boogeyman scare tactics.

My information was that HFCS has a higher “sweetness” to it than regular corn sugar or cane sugar, and that because of this they can use less to gain a similar “sweetness” value. By doing so, they use less raw material per item and save some small amount of calories. Of course, I might have been reading somebody’s propaganda, but I seem to recall something there from food chemistry about it.
Either way, thanks for the article Steve.
Well written, as always.

You’ve got this one wrong Steve. The idea that sugar can cause diabetes is very old-school and largely a myth. There is absolute consensus that sugar in food does not cause diabetes. Type 2 diabetes is strongly inherited, however the main contributing lifestyle factors are lack of exercise and overweight. There is good evidence that high fat consumption promotes insulin resistance. In terms of carbohydrate it is not the quantity of carbohydrate but the quality –ie, rapidly absorbed high GI carbs that are associated with diabetes risk.

studio34 – I agree, that is why I wrote “sugar” and not “carbohydrates”. I know I was glossing over a more complex issue, but generally speaking the simple sugars used as sweeteners have a high glycemic index.

The Men’s Health magazine in 2003 stated that high fructose corn syrup was harder for an athlete to burn off during exercise. Its more slowly metabolized than sugar. Additional public information have claimed this to be true. Is this correct?

HHC- from what I can find this might be true of pure fructose, but not HFCS, which has the same ratio of fructose to glucose as table sugar. Many writers have extrapolated from research using pure fructose to HFCS, and this is not justified.

I’d be curious to know what you think of Gary Taubes and his book, Good Calories, Bad Calories? I found it to be a pretty compelling refutation of the calories-in, calories-out hypothesis. If he’s right, the “scientific consensus” you mention is based on pretty flimsy evidence and all-around bad science.

FWIW, I’m a huge fan of yours and the SGU, so I’m not trying to badger – just genuinely interested in knowing how/if you think Taubes is misrepresenting the state of nutritional science.

I also have an understanding about HFCS (possibly due to bad propaganda) that HFCS has higher solubility than regular sugar and can therefore be packed in at greater concentrations to make food taste sweeter. This is why small portion processed foods that contain HFCS can taste SO good and have SO many calories in them. I believe it’s been discussed on this blog before that people inherently have a poor ability to judge caloric intake, and do so by counting portion quantity rather than portion size. It seems to me that HFCS could very well be contributing to obesity because companies use it to pack so many calories into one small portion. This would similarly be the case even if regular table sucrose was used in lieu of HFCS.

I don’t think this takes the responsibility for calorie-control off of the individual. However, having HFCS in everything certainly isn’t helping the matter. Is there an irrational aspect to this line of reasoning? I’ve been thinking about this topic a bit since hearing Brian Dunning’s take on Skeptoid.

As a registered dietitian, I chuckled, winced, scoffed and said “hmmm…..is there any truth to that?” as I read through all 15 comments to this blog post about high fructose corn syrup (HFCS).

First of all, a big thanks to Dr. Novella for this very informative article and accurate portrayal of this controversial ingredient (HFCS). Second, I’d like to fully disclose my affiliation to this issue, and based on the comments, I think/hope that most will be able to respect my position. I am a nutrition-culinary consultant to food and beverage companies, supermarkets, restaurants and agriculture organizations. And yes, Coca-Cola and the Corn Refiners Association are both clients of mine. My consulting role for ALL my clients is to convey practical, realistic and accurate scientific-based information about food and eating. Often that includes setting the record strait, or at least attempting to, like Dr. Novella has done with this article.

The misinformation and hysteria about HFCS makes my head spin. Whenever someone suggests “removing HFCS from the food supply” as a way to combat obesity, I cringe. As though removing one ingredient will instantly make us all healthier?! I’d like to think/hope that overall lifestyle choices are what will make us healthier – moving more and getting regular exercise/physical activity, staying within your own personal calorie level, making sure you eat the right amounts of all the nutrient-rich food groups to help ward off disease and enjoying decadent desserts, treats and yes – even sugary beverages – in moderation. But this requires effort, discipline and much personal responsibility.

In closing, just a few bits of info about HFCS & Sugar are:
* Practically identical: sugar is 50% fructose and 50% glucose, while HFCS is at most 55% fructose with the remainder being glucose.
* Virtually the same sweetness.
* Metabolized the same way because they are basically the same composition. Your body cannot tell the difference.
* Exactly the same number of calories: 4 calories per gram.

Yes, HFCS is in many of our foods today, but the amount in some foods in very tiny, much like when you and I “add a pinch of sugar” to our homemade spaghetti sauce or salad dressing.” That pinch just seems to help the overall flavor. Even if very tiny amounts are added to food products, it must be listed on the Ingredient Statement.

As to whether food manufacturers are “packing in more HFCS than sugar because of higher solubility” – well that’s out of my league and I suggest a food technologist let us all know if “there is any truth to that.”

Regarding diabetes: Gabriel Cousens advocates a plan based on raw foods and claims to be able to “cure” diabetes in one to several weeks. According to testimonials, people who have taken insulin shots for years or decades have stopped their injections. I am generally skeptical about treatments promoted in this fashion, but is there any evidence that his claims are true, that diabetes can be “cured” by a radically improved diet and exercise regime, assuming that one had the discipline and rigor to stick with the plan?

Dr Novella: Admittedly I was going from a dim recollection of a class in food chemistry, and had no real reference to point to.

Regarding the obesity epidemic :
Back in 1984, I weighed in at 232 lbs. At my height of 6ft 5″, the charts told me that I was considered 12 to 17 lbs overweight.
I had people tell me I looked gaunt or underweight.
This leads me to wonder how much of the “epidemic” is an artifact, and how much of it is actual overweight.

Portion size is important, but portion content is more so.
4oz of lettuce is nothing in calorie content, but 4oz of sugar is quite a bit.
Sorry if I’m stating the obvious here.

I heard something on NPR a few days ago that suggests that, perhaps, a calorie isn’t necessarily the same as all other calories. The researchers had found a correlation (and called it that) between the average amount of processed foods in a population’s diet and the average obesity rates. The research they were talking about was with rats, with two populations living identical lives, except one ate regular uncooked rice, and the other puffed rice. The processing makes the puffed rice easier to digest (the theory goes), and thus costs less metabolic energy to digest. They said the rats living on the puffed rice got fatter than ones on the regular rice.

I’ve also seen the theory that the invention of cooking was a critical moment in the evolution of modern man, because cooking breaks down food and makes it easier to digest, and frees up metabolic energy to support our larger (in proportion to our body size, compared to our primate cousins) brains.

None of the disputes anything in your article, of course, nor would I suggest you are incorrect in your analysis. But it is interesting to see a non-stupid theory that the type of calories can, in fact, make a difference. (Nobody on the program suggested that anything they’ve done so far is conclusive.)

(OK, alcohol is not exactly a nutrient, but for some people is a significant calorie contributor).

That is independent of the composition of said nutrients (that is, wheter a sugar is polymerized glucose, a disaccharide like maltose, lactose or sacarose, or a monosacharide like glucose, fructose or galactose, and the same goes for aminoacid composition in protein and fatty acid composition in fats; that is, for calorie content, these things are important in other ways). That is, fat about twice as much calories as protein and carbohyadrates. I don’t suppose a food can be palatable with more than, say, 30% fat. At that proportion, a food has only 30% more total calories than if it contained only protein or carbohydrates and most foods aren’t that way. The important factor is the proportion of non nutritional components in food, basically, water and non digestible fiber. The problem is that by themselves they aren’t very satisfying because the stomach detects the presence of nutrients in food (mainly fats and proteins) that’s why drinking a lot of water doesn’t make hunger go away. The lettuce example is very telling: lettuce is little more than water and fiber, that’s why if you have herbivore pets (rabbits, guinea pigs, some turtles, iguanas or even fish), feeding them lettuce isn’t recommended, they would end up malnourished. The secret to healthy eating is ingesting enough nutrient rich food to satisfy the stomach, and bulk it up with fiber and water rich foods. So, for instance, you can eat a reasonable portion of a thick steak that has a high proportion of fat, potatoes and the rest can be vegetables than contain mostly water and fiber, a good portion of salad. I’m not an expert in this subject, but the last time I checked in PubMed the latest information and opinions (mainly in reviews), there wasn’t a clear relationship between the glycemic index of foods and type II diabetes. The problem with cereal derived foods, soft drinks and candies, all manily carbohydrates, is that you need to ingest a lot to satify your hunger, whereas if you eat some meat and a lot of vegetables, the TOTAL amount of calories ingested to feel satisfied is quite a bit less.

Before you dismiss HFCS as being equivalent to sucrose, you might look at these numbers. HFCS-55, which sweetens all national brands of soda is 55%fructose:45% glucose. Sucrose is, of course, 50:50. While the difference between the ratio of simple sugars in HFCS-55 and sucrose appears minimal, it really isn’t.
55%:45% = 55/45= 1.22. This means that in every Coke (bottled in the USA) there is, compared to glucose, 22% extra fructose.
Approximately 30% of our ~60lb per capita annual intake of HFCS comes from sweetened beverages. Over time this extra fructose has wreaked havoc on our waistline, livers, and arteries. Dr. Dana Flavin has an excellent summary, “The Metabolic Dangers of High Fructose Syrup”. To your health.

I think that this post oversimplifies the issue a bit.
1. If caloric intake is the issue, then HFCS is still a big part of the problem–it’s in food items it just doesn’t belong in. I recently found out that wheat thins have HFCS in it, and I’ve known for awhile that Friehofer’s sliced breads have it as well. Why?! Because of this, I can’t buy bread at my college campus (the convenience store only sells Friehofer’s) if I want to avoid those extra calories creeping into my diet–I have to drive to the supermarket.

2. (This is notably less important than the above) Sugar and HFCS have different tastes. Anecdotally, I VASTLY prefer the cane sugar sodas that I’ve tried (Jones, Boylan, Mad Dog, to name a few) to anything from Pepsi, Coke, etc. But these premium sodas carry a premium cost.

Weight control is easiest if we don’t eat things processed foods. Eat meat, veggies, fruits. If it is processed, there is a good chance they will sneak things in to harm you — high sugar content (HFCS included) are just one of the many things they try to sneak past the consumer. But as you said, humans lack in will power [and wisdom]. If someone makes something for short term pleasure, we buy it.

– You can “cure” some diabetes (Type II) with diet and exercise, meaning that you can eliminate your need for insulin or even oral medication. This is a standard treatment for diabetes, but is dependent on patient compliance.

– portion size is not “everything”, but, all other things being equal, it is a simple way to reduce caloric intake. But you also need to be aware of the caloric density of your food. So you can also reduce calories by eating not only less food overall but lower calorie food. That is why many people advocate restaurants disclosing calories on their menus.

– Not all HFCS is 55% fructose. Some is 50%. I don’t know the proportion in the industry.

– Re Gary Taubes – he overstates certain aspects of the science. This is a complex issue, so of course my blog post over-simplified. Yes, there are many metabolic factors. But they determine difference among people. For any individual – they cannot radically change their biochemistry, so for them the only real option is to lower caloric intake and increase output – eat less, exercise more.

You can improve your physiology by exercising – so exercise regularly.

For weight loss, the data shows that caloric intake and exercise are the dominant factors. We can argue endlessly about the effects of all the complicated physiological factors having to do with food type – but it just turns out that these effects are too small to detect clinically. Therefore they are probably not relevant for most people.

There are also health concerns separate from weight control, and what you eat matters for those concerns – like heart health, for example.

1. If caloric intake is the issue, then HFCS is still a big part of the problem–it’s in food items it just doesn’t belong in. I recently found out that wheat thins have HFCS in it, and I’ve known for awhile that Friehofer’s sliced breads have it as well. Why?! Because of this, I can’t buy bread at my college campus (the convenience store only sells Friehofer’s) if I want to avoid those extra calories creeping into my diet–I have to drive to the supermarket.

When I have time, I like to make my own. 😉 It’s fun making bread from scratch. I don’t have a breadmaker; I do it the old way. Kneading by hand can be a great way to work off stress.

If you buy bread at the supermarket, it may not have HFCS because it will have refined sugar in it instead. It depends on the type of bread, though. Some breads have more sugar in them than others, and some have to be made with specific sugars. I’m quite partial to honey-wheat bread myself, which of course has honey in it. But they all have to have at least some sugar. The type of sugar isn’t as important, as long as it will feed the yeast. The yeast will convert the sugar into alcohol and carbon dioxide. The alcohol will pretty much all boil off during baking, but the CO2 will be trapped in the bread dough, giving it that wonderful foamy texture we all love. 😉

Adjusting the sugars does affect how that texture turns out, BTW. So there may be a good reason for choosing HFCS instead of granulated sugar. For instance, it may improve the bread’s shelf life by preventing it from drying out too quickly.

As far as flavor, I actually prefer the corn syrup sodas to cane sugar sodas. But that’s just a personal preference thing.

Hi Dr. Novella,
I’ve been hearing more and more about HFCS, starting with the article by Tom Scheve (http://recipes.howstuffworks.com/high-fructose-corn-syrup1.htm) with the corresponding Stuff You Should Know podcast titled “Is high fructose corn syrup bad for you” (uploaded 4-28-2009 by HowStuffWorks.com) followed by Brian Dunning’s podcast (Skeptoid #157) and now your article. What cynthia1770 and the Stuff You Should Know podcast have address and what either Brian Dunning’s or your article have neglected is the ratio of fructose: glucose ratio of HFCS. As far as I can tell, it is a 55:45 for all soda beverages and 42:58 for foods. http://www.newsdesk.umd.edu/sociss/release.cfm?ArticleID=1470

And Dr. Novella, did you actually read the 2004 article or just the summary you linked to? Am J Clin Nutr. 2004 Apr;79(4):537-43. (http://www.ajcn.org/cgi/content/full/79/4/537)
What I’m being to bang my head against the wall is the omission by yourself and others is that fructose and glucose are metabolized differently! I believe it makes a difference. For example, microorganisms such as E. coli and S. cerevisiae will metabolize glucose first and only when glucose is depleted, will they metabolize other carbon sources present. If human metabolism is in anyway regulated the same way (I’d love to know if it’s true or not), than I think it’s noteworthy to look into. Does glucose suppress the rate of fructose converting into glucose by the liver and will the liver respond by storing fructose as triglycerides at a faster rate? and does it make a difference in the long run? The article concludes, “The hypothesis that providing sodas and juice drinks in which caloric sweeteners are partially or completely replaced with noncaloric sweeteners will help reduce the prevalence of obesity is worth testing. ”
I agree that there is no conclusive argument that links HFCS use to obesity but there is a strong correlation. From 2008 review of the literature states: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18924641.
They conclude, “Although observational studies support the hypothesis that sugar-sweetened soft drinks cause weight gain, a paucity of hypothesis-confirming clinical trial data has left the issue open to debate. Given the magnitude of the public health concern, larger and longer intervention trials should be considered to clarify the specific effects of sugar-sweetened soft drinks on body weight and other cardiovascular risk factors.”

Finally, to cherry pick a quote from the SGU website: “multiple independent correlations can point reliably to a causation, and is a reasonable line of argument.” Once good solid studies are completed, will you be willing to change your point of view on HFCS-55, good or bad? In the meantime, I think it’s too early deciding either way. There are persuasive arguments either way. I just have an issue that you omitted the fact that HFCS-55 has more fructose than glucose in soda drinks and that the body metabolizes them different. Sucrose just is not the same as HFCS-55 (as cynthia1770 mathematically pointed out).

To round things out though, is HFCS-42 (used in consumer food) better for you than an equivalent amount of sucrose by following the argument that there is actually less fructose in it that sucrose?
I’m so confused as to what to believe now. Given that I’m a skeptic-in-training, I would great appreciate your critic on my argument and any logical fallacies I’ve made.

As an addendum, in the short term, “metabolic responses are similar to sucrose as would be expected from the composition of these 2 sweeteners.” American Journal of Clinical Nutrition, doi:10.3945/ajcn.2008.25825A Vol. 88, No. 6, 1715S, December 2008.
And… “insufficient scientific evidence currently
exists to indicate that HFCS disrupts short-term energy balance
signals or increases short-term appetite and energy intake more
than do other tested sweeteners. The metabolic and endocrine
responses that have been measured to date are similar between
HFCS and sucrose, the sweetener HFCS has largely replaced in
the US diet. Additional work should be performed to see whether
these results extend to other metabolic and endocrine responses.
In addition, longer-term investigations of the effect of HFCS on
energy balance regulatory systems are needed to further understand
the role of this sweetener in body weight regulation.” Am J
Clin Nutr 2008;88(suppl):1738S– 44S.

Sorry, another thing I thought of, Is my argument considered “moving the goal posts?” The 2004 article presented a long term correlation between obesity and HFCS. The 2008 article (Am J Clin Nutr 2008; 88(suppl): 1715S) presented no short term metabolic difference between HFCS and sucrose. Is demanding good long-term studies to confirm or disprove the short-term findings in order to match up with the 2004 long-term correlation an unrealistic demand?

Draal – I did mention the fact that there are metabolic differences between fructose and glucose. However, the evidence so far suggests that the ratio of fructose to glucose overall in the American diet has not changed, and this is a significant counter argument to the correlational data linking HFCS to obesity.

Yes – correlational data can be compelling, but it is not lining up cleanly in this case. It also would not surprise me at all if there is a legitimate link between sweetened drinks and obesity, but this would not necessarily have anything to do with HFCS, but just with calories. Evidence suggests that drinking calories leads to increased overall caloric intake, and hence obesity – regardless of what form those calories take.

And – of course I would change my opinion if new and reliable evidence suggested otherwise. This story is certainly not over, nor did I imply that it was. Correlational data is always provisional and open to new lines of evidence.

Dr. Novella, thank you for the reply. I agree that intake of extra calories is a major reason for increase in obesity. I would not be surprised either if the average amount of exercise has decrease during the same time. Either way, the point I take from you is that HFCS is not the demon it has been portrayed as but rather the issue is with calorie intake.
I’m a grad student working on metabolic engineering of microorganism so my point of view is to look at small perturbations that can cause large changes in the metabolism in the whole system. Sugars especially have global regulatory impact on metabolism. Basically, i can often get caught up with the details instead of seeing the whole picture.
For further reference, I suggest these two review articles:

The second review is where the relatively unchanging fructose: glucose ratio calculation is coming from. For example the ration was about 0.73 in 1975 and was 0.79 in 2002. I’m going to crunch the numbers again to see if there’s been a change up to 2007.

It seems that every single review has said that there’s no good evidence that links HFCS to obesity BUT proper experiments should be conducted to eliminate the doubt.

I did the number crunching and here’s what I have:http://img43.imageshack.us/img43/6255/fructosegraph.png
As you can see the fructose:glucose levels went from 0.71 in 1975 to 0.80 in 2007. I also graphed the total amount of fructose equivalent consumed. There was a 20% increase in sugar consumed between the same years. I also graphed the % of Americans who are either overweight or obese between 1995 and 2007. all I can say is wow. Just by inspection, there is a week correlation between the fructose:glucose ratio versus % overweight but an opposite trend for total fructose/sugar consumed over the past 10 years. Obesity and calorie intake does track extremely well though (data not shown).

Before you dismiss HFCS as being equivalent to sucrose, you might look at these numbers. HFCS-55, which sweetens all national brands of soda is 55%fructose:45% glucose. Sucrose is, of course, 50:50. While the difference between the ratio of simple sugars in HFCS-55 and sucrose appears minimal, it really isn’t.
55%:45% = 55/45= 1.22. This means that in every Coke (bottled in the USA) there is, compared to glucose, 22% extra fructose.

That’s a really odd way to calculate it, which seems designed to exaggerate the amount of fructose. Why compare it to glucose rather than change in total fructose (5% more fructose)? The only reason to compare fructose to glucose would be if you believed that a molecule of glucose somehow “neutralizes” the supposedly harmful effect of a molecule of fructose.

@trrll
That’s the proper way to calculate a ratio. To be technical, the ratio for HFCS-55 is fructose:glucose being 55:43 = 1.28 (with other stuff making up the missing %). For HFCS-42, the ratio is 42:55 = 0.76. HFCS-55 is used in beverages while HFCS-42 is use as a food additive. The American diet has an approximately 0.80 fructose:glucose make up as of 2008.
And besides, 55%-45% =10%, not 5%. o.O
The American diet is not exclusively sweetened by HFCS. Other sugar sources are sugar cane and beets, glucose/dextrose, honey and edible syrups. The USDA provides a breakdown of commodities produced, imported and sold. This information gives an approximation of the amount of sugars consumed by Americans per capita per year. The info is available here: http://www.ers.usda.gov/Data/FoodConsumption/FoodAvailQueriable.aspx
Fruit and fruit juice also contribute mostly fructose to our diet but the variety of fruit makes it difficult to account for.

What’s been misleading about fructose is that a couple studies conducted on animals on exclusively fructose diets had some serious health issues. HFCS was also introduced in the mid-sixties and became more widely used in the US after 1975 to supplement the use of sucrose. High obesity levels have been linked to the introduction of HFCS. But since HFCS is nearly the same as sucrose in fructose:glucose ratio, the US diet hasn’t changed for all intensive purposes. the actual amount of total sugar has been decreasing for the past ten years but obesity levels still are rising. see my graph: http://img43.imageshack.us/img43/6255/fructosegraph.png
What has changed is an increase from an average 2,100 calories/day in the mid-70s to over 2,700 calories/day today. That’s enough to pack on a few extra pounds.

I need to correct myself…
HFCS with 55% fructose has 10% more fructose content than sucrose (sucrose is 50:50) because 55%/50% = 1.1 or 10% more fructose.

Say you have 55 molecules of fructose and 45 molecules of glucose and compare it to an even 50 and 50 mix. When comparing the two populations, we have 55 vs 50 molecules of fructose. It’s not a 5% difference because if we increased the 50 molecules by 5% we get 52.5 molecules (50*0.05 + 50 = 52.5). If we were to increase the 50 molecules by 10% we get 55 (50*0.10 + 50 = 55).

You really should include other carbohydrates. Many starches are cleaved to glucose in the gut and have as high (or higher) a glycemic index than does sucrose. The glucose from them will dilute the fructose from HFCS.

Our carbohydrate diet has not undergone the same shift in origin of source as our sweeteners. HFCS has replace about 50% use of sucrose. That is why HFCS has grabbed the spot light. It is not a matter of diluting the fructose we consume. There is no benefit from having an extra glucose molecule for every fructose molecule we consume except more calories.
Fructose is metabolized differently by the body than glucose. For example, fructose is primarily processed in the liver where it is turned into either glucose or triglycerides (i.e. fat). Let’s take a hypothetical case: Assume our carbohydrate diet remains unchanged but our sugar diet switches from only sucrose to only HFCS-55. The amount of total fructose is now 10% higher in the new HFCS-55 only diet than the only sucrose diet. The extra amount of fructose the body has to metabolize is what a few researchers and nutritionists concerned. The long term effects is unknown; there has been no proper study conducted on this exact scenario. The short term effects however have shown no difference in the metabolic markers that where measured in the study like insulin, triglyceride levels, ect.

So in short, carbohydrates have stayed the same while sugar sources has changed. Glucose does not cause a dilution effect to offset consumption of fructose.

The other week while watching Biggest Loser, the show which tries to change habits of consumption, the group trainer demonstrated that the average person in the U.S. will consume 500 pounds of sugar from soft drinks alone each year. There was an impressive display of sugar released as a demonstration for quite a few tv minutes.

I checked now the USDA Economic Research Services totals for consumption of cane and beet sugar, edible syrups, honey, HFCS, glucose, and dextrose. The most recent data is from 2007, they estimate the consumption per capita is

The data represents added sugar. It does not include sugar sources such as fruits and fruit juice. Though 500 is awfully far from 150 lbs/year. Maybe if you include the sugar equivalent from starches since they are polysaccharides.

DevilsAdvocate, if you’d like to know what Jenny McCarthy thinks, just check out her vapid thoughts on the subject at her oprah.com blog.

Just so you don’t have to wade through the insipidness, she calls high fructose corn syrup “the devil” and has cut yeast, refined sugar, wheat, dairy, caffeine, alcohol and smoking (fun, enjoyment, pleasure, excitement and anything interesting to talk about) out of her diet.

She also cheerfully adds that she strictly monitors her 7-year-old son’s bowl movements and sends samples of them to labs for testing.

If you can stomach her babbling idiocy, there’s a ton of stuff like these fun little tidbits to make fun of.

Its possible to consume sugary items, such as chocolate due to physiological cravings. Same with polysaccarides, like fried potatoes. If an athlete gives into these cravings performance will be impacted.

Does it bother you that you sound exactly like the woman who works for the corn people? Sorry, one thing I have realized is that when everyone I know who really understands a topic says one thing and all the people who have financial interest say another, I go with the former. Your logic is wonderful but it does sound like you have an agenda to promote. You believe calories are the problem, I think there has to be more to it. Trans fats and high fructose corn syrup are part of the problem. Your source cites the evidence as being “unreliable” and “inconclusive”. Not great denials. I have a great article I could send you. It is an academic piece comparing “Big Food and “Big Tobacco”. The authors, both academics compare the behavior of the food industry to the early tobacco denials etc. My gut is you will live to be wrong on this one. Something has gone drastically wrong in the past generation and it does not “just” come down to calories.

You may also want to check out fructose mediated metabolic syndrome and fructose effects on uric acid levels on PubMed.

E.g. (1) “Dietary fructose and the metabolic syndrome” (Curr Op Gastroenter 24(2):204-209, 2008) and (2) “The effect of high-fructose corn syrup consumption on triglycerides and uric acid” J Nutr. 139(6):1242S-1245S, 2009) where research into those topics is reviewed. The papers come to slightly different conclusions on the contribution from fructose, but do complement the rather selective discussion above.

To quote from said reviews:

(1) “Recent animal studies have confirmed the link between fructose feeding and increased plasma uric acid, a potentially causative factor in metabolic syndrome. … Human studies have demonstrated fructose’s ability to change metabolic hormonal response, possibly contributing to decreased satiety … supporting the notion that fructose is a highly lipogenic nutrient that, when consumed in high quantities, contributes to tissue insulin insensitivity, metabolic defects, and the development of a prediabetic state. Recently evidence has helped to decipher the mechanisms involved in these metabolic changes.”

(2) “Evidence shows that fructose bypasses many of the body’s satiating signals, thus potentially promoting overconsumption of energy, weight gain, and the development on insulin resistance. It has also been shown to increase uric acid levels, which in turn promotes many of the abnormalities seen in the metabolic syndrome including hypertriglyceridemia. … This review highlights the fact that limited data are available about the metabolic effects of HFCS compared with other caloric sweeteners. The data suggest that HFCS yields similar metabolic responses to other caloric sweeteners such as sucrose.”

Keep in mind the economic and political angles to the HFCS discussion in the US. It’s harder for us to grow sugar cane than corn. Consequently the home agricultural companies (especially Archer Daniels Midland) lobbied for tariffs on sugar cane, and it became cheaper to use HFCS than just plain old sugar in drinks (look at soda labels in other countries – it’s more often real sugar; likely for economic rather than health reasons). On top of this, historically Cuba had been the U.S.’s best (i.e. closest ergo cheapest) source for sugar, but after Castro came to power, that door closed as well.

Without getting into conspiracy theories, it seems worth asking why it’s THIS year, after something of a detente with Cuba and some doors opening, that a) the anti-HFCS powers are rallying and b) many drinks are selling a real-sugar version of themselves (Coke, Snapple).

It seems that a comparison with HFCS with sugar is not the correct way to look at this. As Dr. Novella correctly points out biochemically they are metabolized identically. The problem appears to be with fructose (about 50% of sugar and HFCS, the other half being glucose). I recently came across this presentation by Robert H. Lustig, MD, UCSF Professor of Pediatrics in the Division of Endocrinology

The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome
Jung Sub Lim, Michele Mietus-Snyder, Annie Valente, Jean-Marc Schwarz & Robert H. Lustig About the authors

The take away from this is that sugar, and thus fructose, is being added for commercial and business purposes to many foods and this is related to metabolic syndrome and the obesity epidemic. It appears that the advice should not be to “eat in moderation” but to avoid sugar-added foods. The reasoning is difficult to feel satiated by sugar-added foods and expect to consume a “reasonable” amount of fructose.

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Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most frequent liver disease worldwide, and is commonly associated with the metabolic syndrome. Secular trends in the prevalence of these diseases may be associated with the increased fructose consumption observed in the Western diet. NAFLD is characterized by two steps of liver injury: intrahepatic lipid accumulation (hepatic steatosis), and inflammatory progression to nonalcoholic steatohepatitis (NASH) (the ‘two-hit’ theory). In the first ‘hit’, hepatic metabolism of fructose promotes de novo lipogenesis and intrahepatic lipid, inhibition of mitochondrial β-oxidation of long-chain fatty acids, triglyceride formation and steatosis, hepatic and skeletal muscle insulin resistance, and hyperglycemia. In the second ‘hit’, owing to the molecular instability of its five-membered furanose ring, fructose promotes protein fructosylation and formation of reactive oxygen species (ROS), which require quenching by hepatic antioxidants. Many patients with NASH also have micronutrient deficiencies and do not have enough antioxidant capacity to prevent synthesis of ROS, resulting in necroinflammation. We postulate that excessive dietary fructose consumption may underlie the development of NAFLD and the metabolic syndrome. Furthermore, we postulate that NAFLD and alcoholic fatty liver disease share the same pathogenesis.